Malt1^em1Krad

CRISPR/Cas9 technology generated an A to C change resulting in a glutamate to alanine substitution at amino acid 325 (E325A) in the TRAF6 biding motif 1 (T6BM1) in exon 7, an A to C change resulting in a glutamate to alanine substitution at codon 814 (E814A) in the TRAF6 biding motif 2 (T6BM2) in exon 17 of the Malt1a splice variant, and an A to C change resulting in a glutamate to alanine substitution at amino acid 803 (p.E803A) in the T6BM2 of the Malt1b splice variant. These missense mutations render MALT1 incapable of interacting with TRAF6. Differential PCR and genomic and complementary DNA sequencing verified correct genome editing and Western blot analysis showed equivalent protein expression in heterozygous and homozygous T cells as in controls. Loss of TRAF6 biding causes constitutive MALT1 protease activation. (J:333424)